ECG life in the fastlane.pptx

Ecg

1. ECG Quizzes

2. Case 1: Middle-aged patient presenting with chest pain and diaphoresis. BP dropped to 80/50 following sublingual nitrates.

3. Answer General: Sinus rhythm, rate 84bpm. Normal axis. Borderline  1st degree AV block  (PR 220ms). Signs of  inferior STEMI : STE in inferior leads II, III, aVF . Reciprocal STD in lateral leads I, aVL , V6. Signs of associated  right ventricular infarction : STE in III > II. STE in V1-2. This patient also had STE in V4R, confirming the diagnosis of RV infarction:

4. Clinical Pearls RV infarction typically occurs in the context of inferior STEMI due to RCA occlusion. These patients are preload sensitive and may have an exaggerated hypotensive response to nitrates.

5. Case 2: 20-year old female presenting with palpitations and presyncope , BP 75/50.DEscribe her ECG.

6. Answer Main Abnormalities: Irregularly irregular broad complex tachycardia. Extremely  rapid ventricular rates  — up to 300 bpm in places (RR intervals as short as 200ms or 1 large square). Beat-to-beat variability in the QRS morphology, with subtle variation in QRS width. Explanation of ECG Findings: Irregularly irregular rhythm is consistent with  atrial fibrillation . There is a  left bundle branch block  morphology to the QRS complexes. However, the ventricular rate is far too rapid for this to be simply AF with LBBB. The rates of 250-300 bpm and the variability in QRS complex morphology indicate the existence of an  accessory pathway  between the atria and ventricles. Diagnosis: These findings indicate  atrial fibrillation  in the context of  Wolff-Parkinson-White syndrome .

7. Clinical Pearls: Broad complex irregular tachycardia at very rapid rates? -> Suspect AF with WPW! These patients can rapidly become haemodynamically unstable. The options for chemical cardioversion are very limited, favoring DC cardioversion . I would recommend immediate DC cardioversion in this patient. My approach would be to fluid load (0.5 – 1L crystalloid bolus), add in a push-dose pressor to elevate the BP (e.g. metoraminol 0.5 – 1mg IV) sedate with something that has minimal effects on BP (e.g. fentanyl or ketamine in cautious doses), and then shock at 200j biphasic. Consider using an AP pad position for maximal 1st shock success.

8. Case 3: Middle-aged diabetic patient presenting with shortness of breath. Clinical evidence of pulmonary edema . Describe the ECG

9. Main Abnormal Findings Severe bradycardia  of 36 bpm. Rhythm is difficult to ascertain — appears irregular (?slow AF) although there are some small-voltage P waves seen in V1-2. Broad QRS complexes with an  atypical LBBB morphology . Subtle symmetrical peaking (“tenting”) of the T waves in V2-5. Diagnosis The combination of bradycardia, flattening and loss of P waves, QRS broadening and T wave abnormalities is highly suspicious for severe  hyperkalaemia .  This patient had a potassium of 8.0 in the context of anuric renal failure . Clinical Pearls When you see the combination of… Bradycardia Blocks — e.g. AV block, bundle branch blocks Bizarre QRS complexes …. think  hyperkalaemia !

10. Case 4: 20 year old male presenting with seizures. BP 80/50. Describe the ECG.

11. Answer: Main Abnormalities Broad complex tachycardia, rate ~ 130 bpm. The rhythm is likely sinus tachycardia with a  1st degree AV block  — note the  “camel hump”  appearance to the T waves indicating a hidden P wave. Interventricular conduction delay  (QRS duration > 100ms, not typical LBBB / RBBB morphology) Right axis deviation . Secondary R’ wave in aVR > 3 mm. Diagnosis In the context of a patient presenting with seizures and hypotension, the combination of… QRS broadening > 100 ms R’ wave in aVR > 3 mm … is highly suggestive of poisoning with a  sodium-channel blocking agent  — e.g. tricyclic antidepressant. The sinus tachycardia may be due to the  anticholinergic  effects of the TCA.

12. Clinical Pearls  In the context of sodium channel blockade: A QRS duration > 100 ms is predictive of seizures. A QRS duration > 160 ms is predictive of cardiotoxicity. This patient is already manifesting life-threatening toxicity and needs aggressive resuscitation, including: Serum alkalinisation with NaHCO3 to reverse pH-dependent toxicity. Intubation and hyperventilation aiming for alkaline arterial pH (e.g. 7.45 to 7.55). Seizure management with benzodiazepines. BP management with fluid boluses +/- pressors .

13. ECG 005 This following sequence of ECGs is taken from a middle-aged patient presenting with chest pain and diaphoresis. Can you interpret each ECG tracing in the context of the patient’s symptoms? ECG 5a – Chest pain and diaphoresis (time = zero)

14. ECG 5a answer This ECG demonstrates an  anterolateral STEMI ST elevation in V2-6, I and aVL Reciprocal ST depression in III and aVF Pathological Q waves in V2-3 Hyperacute T waves in V2-4 This pattern of changes in consistent with acute occlusion of the  left anterior descending artery .

15. ECG 5b – Resolution of chest pain (t+20 mins)

16. ECG 5b answer There is transient improvement in the ST changes, with development of biphasic T waves in V2-3 . This pattern of T wave changes in V2-3 is known as  Wellens ’ syndrome  and indicates  reperfusion  of a previously occluded LAD artery. The implication of this ECG pattern is that there is an underlying critical LAD stenosis that needs urgent intervention with angiography +/ stenting or CABG.

17. ECG 5c – Recurrence of chest pain (t+25 mins)

18. ECG 5c answer The previously biphasic T waves are now upright again — this phenomenon is referred to as  pseudonormalisation  and is a marker of reocclusion of the culprit artery . Despite temporary restoration of blood flow in ECG 5b, the patient is now re- infarcting !

19. ECG 5d – Ongoing chest pain and diaphoresis (t+35 mins)

20. ECG 5d answer This ECG demonstrates a frank  anterolateral STEMI  with evolving ST changes . This patient had a VF arrest shortly after this ECG was taken, was placed on a mechanical CPR device and taken immediately to the cath lab where she was found to have a 100% proximal LAD occlusion. She was stented, successfully cardioverted and made a good neurological recovery.

21. ECG 006: 30-year old patient presenting with generalized weakness. Describe and interpret the ECG.

22. ECG 006 answer Main Abnormalities The ECG shows widespread ST segment abnormalities . There is a biphasic appearance to the ST segments and T waves, with initial negative deflection (= ST segment depression / T wave inversion) followed by a terminal positive deflection (= U wave). All these waves merge into each other and it is difficult to tell where one wave ends and the other begins. There is gross prolongation of the QU interval (= time from onset of QRS complex to end of T/U wave).

23. Diagnosis  The combination of… Widespread ST depression / T wave inversion Prominent U waves Long QU interval (> 500 ms ) …. is highly suggestive of severe  hypokalaemia . This patient had a serum K of 1.7 mmol /L in the context of decompensated  Conn’s syndrome (primary aldosteronism ) . Clinical Pearls Biphasic T waves may be seen with both myocardial ischaemia ( Wellens ’ syndrome ) and  hypokalaemia . The main differentiating factor (apart from the clinical picture) is the direction of the T waves: Wellens ’ biphasic T waves go UP then down. Hypokalaemic T waves go DOWN then up.

24. ECG 007: 70-year old patient presenting with chest pain, dyspnoea and dizziness. BP 90/50. SaO2 83% RA. Describe the ECG.

25. ECG 007 answer Main Abnormalities Sinus tachycardia ~ 100 bpm. Anterior T wave abnormalities: inverted in V1-3, biphasic in V4. Inferior T wave abnormalities: biphasic in III, aVF . Subtle ST elevation in III and aVF . Significance of ECG Findings This pattern of T wave inversions in the right precordial leads V1-4 plus the inferior leads (especially the rightward-facing lead III) is referred to as the  right ventricular strain pattern . It is a marker of  right ventricular hypertrophy  or dilatation. Diagnosis In a patient presenting with acute shortness of breath, the combination of… Sinus tachycardia RV strain pattern in V1-4 (+/- lead III ) … is highly suggestive of acute cor pulmonale due to massive  pulmonary embolism .

26. However, these ECG changes are not specific to PE and may be seen in other conditions associated with pulmonary hypertension and RV enlargement including: Chronic lung disease  (COPD, lung fibrosis) with chronic cor pulmonale Right ventricular hypertropy  — e.g. due to congenital causes, valvular heart disease Arrhythmogenic right ventricular cardiomyopathy Clinical Pearls Other ECG findings associated with pulmonary embolism include: New  right axis deviation New  right bundle branch block New  dominant R wave in V1 Non-specific ST segment changes The oft-quoted S I  Q III  T III   pattern (deep S wave in lead I, Q wave in III, inverted T wave in III) is neither sensitive nor specific for PE and is infrequently seen (20% of cases). Similarly, sinus tachycardia is not as ubiquitous in PE as people seem to think (< 50% of cases), and certainly should not be relied up to exclude PE.

27. ECG 008: 70-year old patient presenting with severe chest pain, diaphoresis and syncope. BP 65/40.

28. ECG 008 answer Main Abnormalities Widespread ST depression affecting multiple precordial (V2-6) and limb leads (esp. I, II, avF ). To some extent this is masked by an indistinct J point, upsloping (rather than horizontal) ST depression and some baseline wander of the ECG. There is~3 mm ST elevation in aVR .

29. Diagnosis In the context of ischaemic chest pain and cardiogenic shock, the combination of… Widespread ST depression ST elevation in aVR > 1 mm ST elevation in aVR > V1 … is extremely concerning for  left main coronary artery occlusion . However , this pattern is not entirely specific for LMCA occlusion. It may be seen whenever there is diffuse severe subendocardial ischaemia, e.g. Severe triple vessel disease Severe anaemia or hypoxaemia Following resuscitation from cardiac arrest This patient developed progressive cardiogenic shock complicated by runs of  ventricular tachycardia . He was taken for immediate angiography where he was found to have a complete ostial occlusion of his left main coronary artery. 

30. Pitfalls A similar ECG pattern of diffuse ST depression with ST elevation in aVR may also be seen with  supraventricular tachycardias  ( AVNRT  /  atrial flutter ). This  rate-related change  is usually benign and resolves with resolution of the SVT.

31. ECG 009: 55-year old patient presenting with chest pain. Describe the ECG.

32. ECG 009 answer This ECG is an example of  hyperacute anterolateral STEMI : There are markedly peaked, asymmetrical T waves ( = hyperacute T waves ) in V2-5. The  associated loss of R wave height (analogous to early Q wave formation) causes the enlarging precordial T waves to tower over the diminishing R waves. There is also some subtle ST elevation in aVL , indicating  LAD occlusion proximal to the D1 . There are frequent  ventricular ectopic beats , which are concerning in this context as they suggest underlying myocardial irritability and a risk of deterioration to malignant ventricular dysrhythmias such as  VF  or  VT .

33. Serial ECGs of this patient showed evolving anterolateral ST elevation (V1-6, I, aVL ) with development of inferior reciprocal change (lead III).

34. ECG 010: 90-year old patient found on the floor at home. Describe what his ECG shows.

35. ECG 010 answer This ECG demonstrates all the classic features of  hypothermia : Bradycardia Osborne waves (J waves)  = notching at the J point seen in V4-6 Long  QT interval  (~ 600 ms ) Shivering artefact The rhythm is probably  sinus bradycardia  — mapping out the RR intervals reveals a regular rhythm despite the obliteration of the baseline by the shiver artefact.

36. ECG 011: Middle aged female presenting with dyspnoea . Previous mastectomy for breast carcinoma. What does the ECG show?

37. ECG 011 answer Main Abnormalities Sinus tachycardia Low QRS voltages  — Multiple limb lead QRS complexes < 5 mm in amplitude. Electrical alternans  — There is a beat-to-beat variation in the QRS complex height. Taller complexes alternate with shorter ones. The triad of tachycardia, low QRS voltages and electrical alternans is extremely suspicious for  massive pericardial effusion . Given the clinical history, I would be concerned about the presence of a malignant pericardial effusion causing tamponade. The diagnosis can be rapidly confirmed on bedside echo (watch these videos from  The Ultrasound Podcast  to learn how:  Part 1 ,  Part 2 ). There may also be clinical evidence of  pulsus paradoxus .

38. ECG 012: Young male found collapsed at home, apparently intoxicated. What does the ECG show?

39. ECG 012 answer Main Abnormalities Giant T-wave inversions in multiple leads, most prominent in V2-6 Marked  QT prolongation  > 600 ms Diagnosis This ECG pattern is characteristic of  raised intracranial pressure   and is classically seen in the context of  massive intracranial haemorrhage , particularly: Aneurysmal subarachnoid haemorrhage Haemorrhagic stroke

40. Similar ECG patterns have also been reported in patients with raised ICP due to: Large-territory ischaemic stroke causing cerebral oedema (e.g. MCA occlusion) Traumatic brain injury The differential diagnosis for widespread T-wave inversions and QT prolongation includes myocardial ischaemia (e.g.  Wellen’s syndrome ) and electrolyte abnormalities (e.g.  hypokalemia ). However , neither condition would cause the gigantic “cerebral T waves” seen here.

41. ECG 013 : Middle-aged patient presenting with palpitations and dizziness. What does the ECG show?

42. ECG 013 answer Diagnosis This ECG shows a regular broad complex tachycardia with an RSR’ pattern in V1. The differential diagnosis could include: Ventricular tachycardia . SVT with aberrant conduction  — either due to  RBBB  or  WPW . On closer inspection, the ECG demonstrates some classic features of  ventricular tachycardia : Northwest axis  — QRS is positive in aVR , negative in I and aVF . The  taller left rabbit ear  sign — There is an atypical RBBB pattern in V1, where the left “rabbit ear” is taller than the right. Negative QRS complex (R/S ratio < 1) in V6. These findings indicate VT rather than SVT with aberrancy.

43. Clinical Pearls Other factors that increase the likelihood of VT in patients presenting with regular broad complex tachycardia include: Age > 35 (positive predictive value of 85%). Structural heart disease — e.g. IHD, CCF, cardiomyopathy. Family history of sudden cardiac death or arrhythmogenic conditions such as  HOCM ,  Brugada syndrome  or  ARVC  that are associated with episodes of VT. In any patient with a broad complex rhythm, also consider the possibility of toxic / metabolic conditions such as  hyperkalaemia  or  sodium-channel blockade.

44. ECG 014 : Middle aged patient presenting with central chest pain. What does the ECG show?

45. ECG 013 answer Evidence of  inferolateral STEMI ST elevation in the inferior leads (II, III, aVF ) ST elevation in the lateral leads (I, V5, V6) Evidence of  posterior STEMI Horizontal ST depression in V1-4 (maximal in V2-3) Dominant R wave in V2 (R/S ratio > 1) Upright T wave in V2 This pattern of infero - postero -lateral STEMI is most likely caused by occlusion of a dominant left circumflex artery.

46. Look specifically at lead V2 for the combination of Horizontal ST depression. Tall, broad R wave (>30ms wide, R/S ratio > 1) — this is a Q-wave equivalent. Upright T wave — particularly the terminal portion of the T wave. One common trick is to turn the ECG over, hold it up to the light and look through it from behind. This inverts lead V2, which then takes on the appearance of a classic STEMI. Look for evidence of posterior involvement in any patient with an  inferior  or  lateral STEMI . Sometimes it can be difficult to determine whether ST depression in V2-3 is due to posterior STEMI or simply subendocardial ischaemia affecting the anteroseptal wall. The diagnosis can be confirmed by recording  posterior leads V7-9 .

47. ECG 015: Middle aged patient presenting with central chest pain. Posterior leads V7-9. What does the ECG show?

48. (same patient as  ECG 014 ) Posterior leads confirm the presence of posterior wall infarction by demonstrating typical STEMI morphology: ST elevation in V7-9 Q waves in V7-9 Inversion of the terminal portion of the T wave (“ U wave inversion “) in V7-9 How To Record Posterior Leads Simply move the V4-6 electrodes around to the back in the same horizontal plane as V6. Annotate the ECG accordingly. Approximate positions for V7-9 are: V7 – posterior axillary line V8 – tip of scapula V9 – left paraspinal region

49. ECG 016 : 20-year old patient with sudden onset of palpitations. What does the ECG show?

50. Main Abnormalities Narrow complex tachycardia at ~ 150 bpm. Right axis deviation  = just rightward of +90 degrees. Pseudo-R’ waves  in V1-2 = retrograde P waves superimposed on the terminal QRS causing peaking of the  J-point . No clear sinus P waves or  flutter waves  seen.

51. Differential Diagnosis When you see a regular narrow complex tachycardia at 150 bpm, you should think of four main diagnoses: Atrial flutter with 2:1 block  ( especially  in elderly, IHD, CCF) AV-nodal reentry tachycardia  (“SVT”) Orthodromic AV reentry tachycardia  in WPW Sinus tachycardia  — should see P waves but  may be hidden in the T waves  (e.g. with concurrent  1st degree AV block ). There should also be some HR variability compared to the other 3 rhythms. The patient’s young age and presence of retrograde P waves (pseudo R’ waves) suggest a paroxysmal reentry tachycardia involving the AV node — either  AVNRT (“SVT”)  or  orthodromic AVRT . The next step is a therapeutic trial of vagal maneouvres and/or adenosine… (see  Quiz ECG 017 ).

52. ECG 017 : 20-year old patient with sudden onset of palpitations. What does the rhythm strip demonstrate?

53. ECG 017 answer Top rhythm strip Regular narrow complex tachycardia. Pseudo-R’ waves (retrograde P waves) are seen deforming the J point. Middle rhythm strip  12mg adenosine given A salvo of broad and bizarre-looking complexes interrupts the rhythm (this is a common phenomenon during chemical cardioversion with adenosine ) Bottom rhythm strip The patient has reverted to sinus rhythm. The pseudo-R’ waves have now disappeared. There are no obvious  delta waves  of WPW, but this should be confirmed on a 12-lead ECG.

54. ECG 018 : 75-year old patient with narrow complex tachycardia at 150 bpm. Rhythm strip during administration of  IV adenosine. What is happening here?

55. ECG 018 answer In comparison to the  previous example , this patient does not cardiovert to sinus rhythm following an adenosine bolus . Instead, the degree of AV block is transiently increased, revealed underlying  flutter waves  and confirming the diagnosis of  atrial flutter with a 2:1 block .

56. ECG 019 : Middle aged patient presenting with chest pain and diaphoresis. What does the ECG show?

57. ECG 019 answer Diagnosis This combination of ST depression with rocket-shaped T waves in the precordial leads V1-6 is referred to as the De Winter ECG pattern or  “De Winter’s T waves” . It is becoming increasingly recognised as an anterior STEMI equivalent (~2% of LAD occlusions). Some authors  are now recommending that this ECG pattern be treated identically to anterior STEMI, with urgent PCI or thrombolysis. Main Abnormalities ST depression in V2-5, which slopes upwards and joins the ascending limb of the T wave. Prominent, “rocket-shaped” T waves in the precordial leads V2-5. Subtle ST elevation in aVR .

58. Clinical Pearls The De Winter ECG pattern may evolve into (or even evolve from) a more classic STEMI pattern.

59. ECG 020 : 80-year old patient with palpitations and syncope. What does the ECG show?

60. ECG 020 answer Main Abnormalities Runs of tachycardia are interspersed with long sinus pauses (up to 6 seconds). The sinus rate is extremely slow, varying from 40 bpm down to around 10 bpm in places. Sinus beats are followed by paroxysms of junctional tachycardia at around 140 bpm. Diagnosis This is a good example of  sick sinus syndrome  leading to the  tachycardia-bradycardia syndrome . The flurries of junctional tachycardia are a compensatory phenomenon attempting to maintain cardiac output in the face of critically low sinus node rates. The syncope likely occurred due to a long sinus pause with temporary loss of cardiac output. This patient needs a pacemaker!

61. ECG 021 : 75-year old smoker presenting with acute dyspnoea and productive cough. Describe the ECG.

62. ECG 021 answer This ECG demonstrates many of the features of  chronic pulmonary disease : Rightward QRS axis (+90 degrees). Peaked P waves in the inferior leads > 2.5 mm ( P pulmonale ). Rightward P-wave axis (inverted in aVL ). “Clockwise rotation” of the heart with a delayed R/S transition point (transitional lead = V5 ). Absent R waves in the right precordial leads (SV1-SV2-SV3 pattern). Low voltages in the left-sided leads (I, aVL , V5-6). Tachycardia may be due to dyspnea, hypoxia or beta-agonist treatment.  T his ECG pattern is a common finding in patients with COPD. The vertical axis (+90 degrees) is due to hyperinflation of the lungs causing vertical orientation of the heart.

63. ECG 022 : Post-intubation ECG of a young adult presenting with coma following a 6g quetiapine overdose. Describe the ECG.

64. ECG 022 answer Main Abnormalities This ECG displays the characteristic electrocardiographic features of  quetiapine toxicity : Sinus tachycardia  due to  anticholinergic  effects. Prolonged QT interval  (QT interval > half the RR interval; QTc = 560ms). A similar pattern would be seen with other atypical antipsychotic agents such as olanzapine or clozapine. Significance of QT prolongation QT prolongation is a common source of concern in patients with antipsychotic toxicity, because of the theoretical risk of  Torsades de Pointes. A QTc interval > 500 ms is commonly cited as a marker of increased risk of TdP . However, tachycardia (which is almost ubiquitous in significant poisoning with quetiapine, olanzapine or clozapine) is actually protective against  TdP . For this reason, TDP rarely occurs with quetiapine toxicity.

65. By my measurements, our patient has an absolute QT of ~320 ms with HR 120 so plots below the line — i.e.  not  at significant risk of TdP . QT interval nomogram Many Australian toxicologists use the  QT interval nomogram  to assess risk of TdP . The  absolute QT interval is measured manually in multiple leads and the median QT interval plotted on the nomogram ( read how to do this here ). Plots  above the line indicate significant QT prolongation and consequent risk of TdP .

66. ECG 023: Elderly patient with accidental overdose of sotalol . Describe the ECG.

67. ECG 02 3 answer Main Abnormalities This ECG demonstrates the key features of sotalol toxicity: Sinus bradycardia (42 bpm) Very long QT interval (~600 ms ). Sotalol is a beta blocker with additional class III effects (potassium channel blockade), so it causes both bradycardia and QT prolongation in overdose . Risk of Torsades In comparison to the  previous case , this patient is at significant risk of TdP . The combination of bradycardia and significant QT prolongation means that this patient plots well above the “at risk” line on the QT nomogram. Prophylaxis of TdP  in this case would include correction of QT-dependent electrolytes (K, Mg, Ca) to the high-normal range and positive chronotropy (e.g. with isoprenaline ) to move the patient below the at-risk line.

68. ECG 024 : Asymptomatic adult patient. Routine ECG. Describe the ECG.

69. ECG 02 4 answer Main Abnormalities This ECG demonstrates the typical features of  dextrocardia : Marked  right axis deviation  (+180 degrees). Lead aVR : Positive QRS complex (upright P and T waves). Lead I: inversion of all complexes, aka ‘global negativity’ (inverted P-QRS-T). Absent R-wave progression in the chest leads (dominant S waves throughout). Differential Diagnosis Accidental  reversal of the left and right arm electrodes  may produce a similar picture to dextrocardia in the limb leads, but with normal appearances in the precordial leads.

70. ECG 025 Asymptomatic adult patient. Routine ECG. Describe the ECG. :

71. ECG 02 5 answer Main Abnormalities This ECG is a classic example of limb lead misplacement with a  left arm / right arm lead reversal : Positive P-QRS-T in lead  aVR . Inverted complexes in leads I and aVL . Normal complexes in the precordial leads rules out  dextrocardia  (compare this to the  previous ECG ). The most obvious abnormality on this ECG is the positive QRS complex in aVR . This is unusual and should always prompt a search for additional evidence of limb lead misplacement. Effects of LA-RA lead reversal Switching the LA and RA electrodes produces the following effects: Lead I becomes inverted. Leads II and III switch places. Leads aVL and aVR switch places (hence aVR becomes positive, aVL negative). Lead aVF remains unchanged

72. ECG 026 : 70-year old patient presenting with chest pain and diaphoresis. Describe the ECG.

73. ECG 02 6 answer This is a very worrying ECG demonstrating massive  anterolateral STEMI  with “tombstone” morphology: Gross ST elevation in V1-6, I and aVL . Early Q wave formation in aVL . Reciprocal ST depression in inferior leads II, III and aVF . This ECG pattern is seen in proximal LAD occlusion and indicates a large territory infarction with a poor LV ejection fraction and high likelihood of cardiogenic shock and death.

74. ECG 027 : Elderly patient feeling generally unwell. PMHx of T2DM, hypertension, IHD, CCF, osteoarthritis. Describe the ECG.

75. ECG 02 7 answer Main Abnormalities Bizarre appearing complexes. Marked T wave peaking in V2-6. Gross QRS prolongation (~200 ms ). Some leads (I, aVR ) are starting to take on a sine wave appearance. Diagnosis The combination of… Bizarre complexes QRS prolongation Peaked T waves Sine wave appearance … are all strongly suggestive of  severe hyperkalemia . This patient had a serum K of 9.2 mmol /L! In this elderly patient with multiple medical problems, causes could include renal failure (e.g. due to diuretics, NSAIDs, intercurrent illness) or treatment with ACE-inhibitors, spironalactone or K-supplements.

76. ECG 028 : 30-year old Thai male presenting with syncope. Describe the ECG .

77. ECG 02 8 answer ECG Findings The patient is in sinus rhythm with no evidence of dysrhythmia or AV block. The   QT interval  is normal and there is no evidence of  WPW syndrome ,  HOCM  or  ARVC . There is a characteristic pattern of abnormalities in V1-2: RSR’ pattern / partial RBBB . ST elevation with a “coved” morphology. Inversion of the terminal portion of the T wave. In a patient presenting with syncope, this ECG is diagnostic of the  Brugada syndrome .

78. Syncope ECG Checklist When faced with a patient presenting with syncope, I systematically assess the ECG for the following abnormalities (click each item for details): Too Fast? Too Slow? Pump Failure Syncope Syndromes Electrical Problems

79. ECG 029 : Asymptomatic 40-year old patient. Describe the ECG .

80. ECG 02 9 answer Main  Findings Irregular narrow-complex rhythm ( overall rate = 72 bpm ). Normal sinus P waves  are seen (upright in lead II), indicating a sinus origin of the rhythm. QRS complexes cluster in groups, separated by non-conducted P waves. The PR interval progressively prolongs within each group. The PR prolongation can be appreciated by comparing the first and last PR interval of each group. Diagnosis   This is the typical appearance of  2nd degree AV block with Mobitz I conduction ( Wenchebach phenomenon) . Clinical Significance In comparison to patients with  Mobitz II , who typically require a pacemaker for prophylaxis of  complete heart block  and ventricular standstill, patients with Mobitz I do not necessarily need any intervention. This is provided that they are asymptomatic with a normal BP, and that reversible causes such as drug toxicity ( beta-blockers ,  digoxin ),  hyperkalaemia  and  myocardial ischaemia  have been excluded. The risk of progression to haemodynamically unstable AV block in these patients is very low.

81. ECG 030 : 85-year old patient presenting with nausea, vomiting and visual disturbance. Looks clinically dehydrated. Describe the ECG.

82. ECG 030 answer Main Abnormalities Atrial tachycardia , with regular P waves visible at ~ 160 bpm (many of the P waves are hidden within T waves and VEBs). Evidence of  high-grade AV block  — there is a 4:1 conduction ratio between P waves and QRS complexes, with a QRS rate of ~ 40 bpm. Frequent ventricular ectopic beats occurring in a pattern of  ventricular bigeminy . Alternating LBBB and RBBB morphology , with the conducted QRS complexes demonstrating  RBBB morphology  (RSR’ in V1) and the VEBs demonstrating  LBBB morphology  (dominant S wave in V1).

83. Diagnosis The combination of… Atrial tachycardia Frequent ventricular ectopic beats High-grade AV block … is almost pathognomonic of  severe digoxin toxicity .

84. ECG Features of Digoxin Toxicity Digoxin toxicity produces a wide variety of dysrhythmias, due to: Increased automaticity  of atrial and ventricular tissues — via actions at the Na/K and Na/Ca exchangers causing increased intracellular calcium and therefore increased spontaneous depolarisation of cardiac pacemaker cells. Decreased AV conduction  — via increased vagal tone at the AV node. Digoxin toxicity therefore usually produces some combination of: Increased atrial automaticity  — especially atrial tachycardia, but also  atrial ectopics ,  AF ,  flutter . Increased ventricular automaticity  —  frequent VEBs and bigeminy ,  polymorphic VT . AV blocks  — including  1st ,  2nd  and  3rd degree  AV block. Characteristic ECG patterns include: Atrial tachycardia with high-grade AV block  (= the classic dig-toxic rhythm). “ Regularised AF”    =  AF with complete heart block + accelerated junctional escape rhythm, producing a paradoxically regular rhythm. Bidirectional VT  = polymorphic VT with QRS complexes that alternate between left- and right-axis-deviation, or between LBBB and RBBB morphology. NB. Digoxin toxicity should not be confused with  digoxin effect  (= “sagging” ST depression and T-wave inversion in patients on therapeutic doses of digoxin; not predictive of toxicity). 

85. ECG 031 : Young adult patient presenting with syncope. History of eating disorder. Describe the ECG.

86. Main Abnormalities The first half of the ECG shows sinus rhythm with  prominent U waves  and a  long QU interval  (520ms). An  atrial ectopic beat  kicks off a run of  Torsades de Pointes  by landing on the T/U wave during the vulnerable phase of repolarisation and causing “R on T” (or “R on U”) phenomenon ECG 031 answer Diagnosis The combination of… Atrial ectopy Prominent U waves Long QU interval Torsades de Pointes … is strongly suggestive of  severe hypokalaemia . This patient had a K of 1.9 mmol /L.

87. Hypokalaemia occurs in eating disorders via multiple mechanisms including: Loss of K+ in bodily secretions — vomiting, purging with laxatives or diuretics. Reduced oral intake. Metabolic alkalosis from vomiting causing intracellular shifts of K+. Hypovolaemia  causing secondary aldosteronism with renal loss of K+. U wave morphology The appearance of U waves in hypokalemia may vary. This example demonstrates discrete U waves that are clearly distinguishable from the T wave. Compare this with  Quiz ECG 006 , where the whole ST-T-U complex is fused together to produce a “rollercoaster” appearance, with the U wave appearing as a positive deflection that emerges from a negative ST segment and T wave .

88. ECG 032: Young adult patient with pleuritic chest pain. Describe the ECG.

89. ECG 031 answer Main Abnormalities This ECG demonstrates many of the classic features of  acute pericarditis : Widespread concave ST elevation with PR depression — most notable in I, II, III, aVF , V5-6. PR elevation in the inverted leads aVR and V1. Downward sloping of the TP segment =  “ Spodick’s sign” . No reciprocal changes of STEMI. ST segment / T wave ra tio > 0.25  ( favours pericarditis over  BER )

90. Pericarditis versus Benign Early Repolarisation Pericarditis can be difficult to differentiate from  BER  as both conditions are associated with concave STE. One useful trick to distinguish between these two entities is to look at the  ST segment / T wave ratio . The amplitude of the STE (from PR segment to J point) is measured in V6 and compared to the T wave amplitude. A ratio of > 0.25 suggests pericarditis A ratio of < 0.25 suggests BER Example 1: Benign Early Repolarisation ST segment height = 1 mm T wave height = 6 mm ST / T wave ratio = 0.16 The ST / T wave ratio < 0.25 is consistent with BER . Example 2: Pericarditis ST segment height = 2 mm T wave height = 4 mm ST / T wave ratio = 0.5 The ST / T wave ratio > 0.25 is consistent with pericarditis.

91. ECG 033: 75-year old patient presenting with acute dyspnoea , productive cough and wheeze. Describe the ECG.

92. ECG 033 answer Main Abnormalities Irregularly irregular narrow-complex tachycardia at ~ 110 bpm. At least 3 different P wave morphologies seen in the lead II rhythm strip, indicating multiple foci of activity within the atria. No flutter or fibrillatory waves — rules out  AF  or  flutter with variable block . Evidence of  right ventricular hypertrophy  —  RAD ,  dominant R wave in V1 , deep S wave in V6. Diagnosis   The combination of… Irregular narrow-complex tachycardia (> 100 bpm) Multifocal atrial activity (3 or more distinct P wave morphologies) No evidence of flutter / AF … is diagnostic of  multifocal atrial tachycardia (MAT) . ECG changes of  right ventricular hypertrophy  may represent  cor pulmonale  due to  COPD

93. Clinical Significance MAT typically occurs in patients with severe COPD, as the final common pathway of multiple arrhythmogenic mechanisms: Right atrial dilatation  (from  cor pulmonale ) . Increased sympathetic drive — due to hypoxia / hypercarbia. Bronchodilators — beta-agonist, theophylline. Electrolyte abnormalities —  hypokalaemia  and  hypomagnesaemia  (e.g. secondary to diuretics / beta-agonists ). MAT typically resolves with treatment of the underlying COPD exacerbation and correction of any electrolyte abnormalities, although it may evolve into AF or flutter.

94. ECG 034: Middle-aged patient presenting with chest pain. Describe the ECG .

95. ECG 034 answer Main Abnormalities The ECG changes are partially masked by the presence of a  right bundle branch block , but there is clear evidence of  anteroseptal STEMI : Gross ST elevation in V1-3 (~ 5mm in V2). Convex ST elevation in I and aVL . Reciprocal ST depression and T wave inversion in the inferior leads (II, III, aVF ). Predicting the Site of LAD Occlusion This ECG demonstrates some markers of a  very proximal LAD occlusion , involving the two most proximal branches of the LAD — the first septal branch (S1) and the first diagonal branch (D1). Signs of occlusion proximal to S1 ( Signs of basal septal involvement) : New RBBB — occurs due to septal infarction ST elevation in V1 > 2.5 mm ST elevation in aVR   ST depression in V5 Signs of occlusion proximal to D1 ( Signs of high lateral involvement) : ST elevation in aVL Inferior reciprocal ST depression > 1 mm 

96. A Common Pitfall  This STEMI pattern is occasionally missed, when clinicians erroneously attribute the ST segment changes in V1-3 to RBBB alone. However, the two patterns are quite different: Typical RBBB will have ST depression and TWI in V1-3 . Superimposed septal STEMI will lead to ST elevation, Q wave formation, loss of the initial R wave and inversion of only the terminal portion of the T wave. This patient arrived by ambulance following an out-of-hospital VF arrest and was taken straight to the cath lab where he was found to have a complete ostial occlusion of his LAD.

97. ECG 035: 80-year old patient presenting with syncope. Describe the ECG .

98. On first glance this ECG could easily be mistaken for an example of  Mobitz II AV block  — there are intermittent non-conducted P waves with a constant PR interval. However, regular  pacing spikes  can be seen following the P waves in leads V3-6. This is an example of  pacemaker malfunction , with intermittent  failure to capture : Regular P waves are seen at ~65 bpm . Each P wave is following by a pacing spike (best seen in V3-6, subtle pacing spikes also present in I, aVR , V1). This indicates that  atrial sensing  is intact.  NB. Pacing spikes will typically not be seen in all 12 leads.  Some of the pacing spikes are followed by typical  ventricular-paced  complexes. The  LBBB morphology  indicates that the pacing lead is in the right ventricle — the heart depolarises from right to left in the same way as LBBB. Also note the  negative concordance  in V1-6 (all QRS complexes are negative). This is often quoted as a feature of  ventricular tachycardia , but simply indicates that the rhythm is arising from the anterior surface of the right ventricle — the heart is depolarising   away  from the V1-6 electrodes.

99. Failure to Capture The problem here is failure of the pacemaker to “capture” ( depolarise ) the ventricular myocardium. Causes of this include: Pacemaker lead fracture or migration (e.g. due to  Twiddler’s syndrome ). Refractory myocardium — due to electrolyte abnormality (esp.  hyperkalaemia ) or  myocardial ischaemia . Several of the P waves / pacing spikes are not followed by QRS complexes, producing a ventricular rate of ~ 40 bpm. Quite worryingly, there does not seem to be any native ventricular activity kicking in when the heart rate drops. The second half of the rhythm strip shows two sequential non-conducted P waves with no evidence of any  escape rhythm . This suggests the presence of underlying  complete heart block  with inadequate escape mechanisms and significant risk of ventricular standstill.

100. ECG 036: Middle-aged patient presenting with chest pain. Describe the ECG .

101. Main Abnormalities This ECG is a good example of  high lateral STEMI : ST elevation is confined primarily to the high lateral leads I and aVL . There is reciprocal ST depression in the inferior leads II, III and aVF . The deep Q waves and poor R wave progression in V1-4 suggest prior  anteroseptal infarction  or  dilated cardiomyopathy . High lateral STEMI is classically associated with occlusion of the  first diagonal branch (D1) of the LAD , but may also occur with occlusion of the obtuse marginal branch (OM) of the circumflex artery, or the ramus intermedius. Clinical Pearls  High lateral STEMI may be extremely subtle. Sometimes the only clue is the presence of new inferior ST depression. Such localised ST depression should always be considered to be reciprocal change rather than “inferior ischaemia” as  subendocardial ischaemia does not localise .

102. ECG 037: 15-year old patient presenting with rapid palpitations and dizziness. Symptoms resolved en route to hospital. Describe the ECG.

103. Main Abnormalities This ECG is diagnostic of the  Wolff-Parkinson-White (WPW) syndrome : Sinus rhythm with a very  short PR interval  (< 120ms). Broad QRS complexes. Delta waves  = slurred upstroke to the QRS. Other Features: Dominant S wave in V1 — this “type B” pattern indicates a right-sided accessory pathway. Tall R waves and inverted T waves mimic the appearance of  LVH  — this is an electrical phenomenon due to WPW and not a sign of ventricular hypertrophy. ST segments and T waves show typical “discordant” changes — they point in in the opposite direction to the QRS complex, similar to  LBBB .

104. ECG 038: 15-year old patient presenting with rapid palpitations and dizziness. Symptoms recur in ED. Describe the ECG.

105. Main Abnormalities Very rapid, regular broad-complex tachycardia (~ 200 bpm ). LBBB morphology (dominant S wave in V1 ). No clear atrial activity — no flutter waves or fibrillatory waves. No obvious  diagnostic features for VT . Differential Diagnosis In a patient presenting with a regular broad-complex tachycardia and no evidence of atrial activity, the main diagnostic considerations are: Ventricular tachycardia . SVT  with aberrant conduction due to  bundle brach block . SVT  with aberrant conduction due to  WPW . Although  diagnostic criteria  exist to aid in differentiation of these rhythms, none of them have 100% sensitivity or specificity — leading many authors to recommend treating as VT if uncertain. However, clinical context is everything… This patient has two strong indicators of SVT with aberrancy: Young age — the vast majority of BCTs in children are SVT with aberrancy. Evidence of WPW on  previous ECGs .

106. Diagnosis This is an example of  antidromic AV reentry tachycardia  — a reentrant SVT seen in WPW where the impulse travels from atria to ventricles via the accessory pathway, recycling backwards through the AV node (hence “ antidromic ”). Activation of the ventricles via the accessory pathway produces a broad complex that may be indistinguishable from VT. This is in comparison to orthodromic SVT, where the impulse travels forwards through the AV node producing a normal-looking, narrow QRS . This patient reverted back to sinus rhythm with vagal maneouvres . The WPW pattern was once again visible on his  sinus rhythm ECG .

107. ECG 039: Elderly patient presenting with chest pain. BP 80/50. Describe the ECG.

108. This ECG shows extensive  infero - postero -lateral STEMI  with “tombstone” morphology: Gross ST elevation in II, III, aVF  consistent with  inferior infarction . Reciprocal ST depression seen in I, aVL . ST elevation in V5-6 indicating  lateral wall involvement . ST depression in V2 is suggestive of associated  posterior wall infarction  — the morphology is the exact inverse of the ST elevation in the inferior leads . There are some additional features suggest of  right ventricular infarction : STE in lead III > lead II. Deep ST depression in V2 with an isoelectric ST segment in V1. This is a huge infarct with a likely poor prognosis. Hypotension may be due to nitrate therapy causing exaggerated preload reduction in the context of RV infarction, or may simply reflect the large infarct size with development of early cardiogenic shock

109. ECG 040: 36-year old old athlete, asymptomatic. Describe the ECG.

110. See additional ECG for this patient

111. Main Abnormalities There are two competing rhythms at similar rates (= isorhythmic AV dissociation): Accelerated idioventricular rhythm  (AIVR) — broad-complex ventricular rhythm at around 60 bpm. Sinus bradycardia  with  sinus arrhythmia  — the sinus rate varies from 70 bpm down to < 50 bpm . The QRS morphology varies depending on which focus is capturing the ventricles at any given moment. Other Findings Specific ECG findings that confirm the presence of simultaneous sinus and ventricular rhythms are: Capture beats — sinus beats that intermittently wrest control of the rhythm producing narrow complexes. Fusion beats  (seen in the second ECG) — these are intermediate width complexes that occur when sinus and ventricular beats coincide. NB . Fusion and capture beats are often discussed in the context of VT. They are not specific to VT, but rather can be seen with any ventricular rhythm, including  paced rhythms  and  AIVR .

112. Explanation Competing sinus and ventricular pacemakers are present. There is underlying sinus arrhythmia, with sinus capture occurring when the sinus rate exceeds the idioventricular rate. This patient was a fit athlete with presumably high resting vagal tone that suppressed his sinus node output and allowed an ectopic ventricular pacemaker to emerge. Definitions Accelerated idioventricular rhythm An ectopic ventricular rhythm consisting of three or more ventricular complexes occurring at a rate of 50-110 bpm. The rate differentiates AIVR from  ventricular escape rhythms  (rate < 50 bpm) and  VT  (> 110bpm). Isorhythmic AV dissociation AV dissociation with sinus and ventricular complexes occurring at similar rates, unlike  3 rd degree heart block  where the atrial rate is usually faster than the ventricular rate.   Isorhythmic AV dissociation is usually due to functional block at the AV node from retrogradely conducted ventricular impulses (“interference-dissociation”), which leaves the AV node refractory to the anterograde sinus impulses.

113. ECG 041: 70-year old patient presenting with acute pulmonary edema . Describe the ECG

114. This is an ECG example of  dilated cardiomyopathy  demonstrating signs of enlargement of all four cardiac chambers: There is marked  LVH  with very deep S waves in V2-4. Right axis deviation  suggests associated  RV enlargement  (=  biventricular enlargement ). Evidence of  left atrial enlargement  (deep, wide terminal portion of the P wave in V1). Peaked P waves in lead II suggestive of  right atrial enlargement  (~ 2.5mm in height ). This patient had four-chamber dilatation on echocardiography with severe congestive cardiac failure (awaiting cardiac transplantation).

115. ECG 042: 75-year old patient presenting with palpitations. Describe the ECG

116. Main Abnormalities  This is a typical example of  atrial flutter with 2:1 AV block Narrow complex tachycardia at 150 bpm. Sawtooth flutter waves are seen in the inferior leads II, III, aVF . Upright flutter waves in V1 appear either as pseudo-P waves or as notches in the T wave. There is a clear 2:1 relationship between the flutter waves (300 bpm) and QRS complexes (150 bpm)

117. Tips for Spotting Atrial Flutter Suspect flutter with 2:1 block in any patient with a regular NCT at 150 bpm. Scrutinise leads II and V1 for flutter waves. Flutter waves are typically sawtooth in lead II and resemble P waves in V1. Try turning the ECG upside down — this can make the flutter waves in lead II easier to see.

118. ECG 043: Middle-aged patient presenting with syncope. Describe the ECG

119. Main Abnormalities Sinus rhythm with evidence of  2nd degree AV block The QRS complexes cluster in groups separated by non-conducted P waves. There is a 3:2 relationship between the P waves and QRS complexes. With   fixed ratio blocks  like this, it can sometimes be difficult to distinguish between  Mobitz I  and  Mobitz II  conduction, as there are not always enough successive PR intervals to judge whether progressive PR prolongation is occurring. The PR interval seems relatively constant between the first and second beats of each group, suggesting  Mobitz II  conduction. However , the clustering of QRS complexes into repeating groups with P:QRS ratios of 3:2, 4:3, 5:4, etc. is a characteristic feature of  Mobitz I . There is an  atypical RBBB  — typical RSR’ pattern in V1 with slurred S wave in lead I, but atypical morphology elsewhere.

120. Pragmatically, I wouldn’t get too focussed on trying to work out the rhythm from a single tracing. I would just record multiple ECGs aiming to capture any longer P:QRS cycles to assess whether successive PR prolongation is present ( Mobitz I ) or absent ( Mobitz II ).

121. Another clue to aid differentiation is QRS width: Mobitz I is typically due to block at the level of the AV node — hence QRS complexes are usually (but not always) narrow. Mobitz II typically occurs on a background of widespread conducting system disease ( LBBB  or  bifascicular block ). The block is typically at the level of the fascicles — hence QRS complexes are usually (but not always) broad. Clinical Pearls There is some prognostic value in differentiating between Mobitz I and II — Patients with Mobitz II have a much higher rate of complete heart block and are more likely to require a permanent pacemaker. However , in the acute situation it is more important to  look at the patient  rather than to fixate on the ECG. Treatment decisions such as whether to commence temporary pacing will be largely determined by the patient’s clinical stability.

122. ECG 044: Middle-aged patient presenting with syncope. Becomes hypotensive in ED (BP 80/50). Describe the ECG

123. There is sinus rhythm with  complete heart block : Normal P waves  (upright in II, inverted in aVR ) are present at a rate of ~ 85 bpm. There is no relationship between the P waves and QRS complexes — the PR intervals vary randomly. A  ventricular escape rhythm  is present at ~ 36 bpm. The broad QRS complexes, RBBB morphology and left axis deviation (resembling  trifascicular block ) indicate a ventricular escape rhythm arising in the left posterior fascicle. Note how the QRS axis and morphology have changed significantly from the  previous ECG . This patient had complete heart block due to  cardiac sarcoidosis Clinical Pearls Sarcoidosis should always be considered as a differential diagnosis in younger patients presenting with complete heart block, particularly if other manifestations of sarcoidosis are present such as  bilateral hilar lymphadenopathy  or  cutaneous lesions  (erythema nodosum , lupus pernio ). One of the most common reversible causes of complete heart block is  severe hyperkalaemia  — always get an urgent K+ (e.g. run a VBG) on patients presenting with CHB. You look a bit silly inserting an unnecessary pacing wire when you could have corrected the problem with some calcium gluconate!

124. Causes of Complete Heart Block AV nodal blocking drugs ( e.g. calcium -channel blockers ,  beta-blockers ,  digoxin ) Severe  hyperkalaemia . Inferior myocardial infarction  — due to increased vagal tone.  Anterior myocardial infarction  — due to septal necrosis. Idiopathic fibrosis of the conducting system ( Lenegre’s or Lev’s disease). Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair) Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis). Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease). Autoimmune (SLE, systemic sclerosis)

125. ECG 045: 64-year old female presenting with severe chest pain and diaphoresis. Describe the ECG

126. This ECG shows a  ventricular paced rhythm  with positive  Sgarbossa criteria : There is  concordant ST depression  in V2-5. This violates the  expected pattern of discordance  for a V-paced rhythm and is a marker of superimposed  myocardial infarction . The morphology in V2-5 is reminiscent of  posterior STEMI , with horizontal ST depression and prominent upright T waves. Multiple non-conducted P waves are seen, indicating the presence of underlying  high-grade AV block  (probably the indication for pacemaker insertion). However, the  fusion complex  (beat #5 on rhythm strip) suggests that P waves are occasionally transmitted, arguing against  complete heart block . This patient did indeed have an isolated  posterior infarction , due to complete occlusion of a posterolateral branch of the RCA. She was successfully treated with PCI. Sgarbossa Criteria These criteria allow for detection of myocardial infarction in patients with  LBBB  and  V-paced rhythms  (previously thought to be “impossible”).

127. Normal Pattern in LBBB / VPR The expected finding in patients with uncomplicated LBBB / V-paced rhythm is  discordance  — i.e. the ST segments and T waves point in the opposite direction to the QRS complex How To Spot Superimposed MI Superimposed myocardial infarction is suspected if there is either: Loss of the usual pattern of discordance — i.e.  concordant ST changes. Excessive discordant ST elevation  — i.e. out of proportion to what would be expected for LBBB / paced rhythm.

128. Sgarbossa Criteria Diagnosis of MI in LBBB / VPR requires at least one of the following criteria to be present: Concordant ST depression > 1 mm in V1-3. Concordant ST elevation > 1 mm in any lead. Excessively discordant ST elevation in any lead >5 mm (original Sgarbossa criteria) or >25% of the corresponding S-wave depth ( modified Sgarbossa criteria  = more specific). Changes only have to be present in a single lead to be diagnostic of MI

129. ECG 046: Middle-aged patient presenting with palpitations. Describe the ECG

130. This ECG contains multiple diagnostic features for  ventricular tachycardia : Regular broad complex tachycardia at ~150 bpm. Very broad QRS complexes (~200 ms ). Northwest axis  (-120 degrees) with positive QRS in aVR . Brugada’s sign – Time from onset of the QRS complex to nadir of the S-wave > 100ms. Josephson’s sign – Notching near the nadir of the S wave. Also note the presence of morphology criteria favouring VT over RBBB: Tall monophasic R wave in V1. Dominant S wave in V6

131. This pattern in V1 and V6 is very different from the expected morphology in RBBB Tips for Spotting VT when RBBB morphology present [NB. RBBB morphology = QRS > 120ms with dominant R wave in V1] Suspect VT in any patient with a regular broad complex tachycardia (especially if > 160 ms wide). Look at aVR - Positive QRS complex? - Leads I and aVF negative? - If yes to both ->  northwest axis  is present -> probable VT. Look at V1 Monophasic R wave or  taller left rabbit ear ? -> probable VT. RSR’ pattern with taller right rabbit ear? -> possible SVT with RBBB.

132. Look at V6 Dominant S wave (R/S ratio < 1)? -> probable VT. Dominant R wave with wide slurred S wave -> possible SVT with RBBB. If still uncertain… scrutinise the ECG for: Brugada’s and Josephson’s signs (see above). AV dissociation — P waves randomly deforming the QRS complexes and T waves. Fusion and capture beats.

133. ECG 047: Middle-aged patient presenting with palpitations. Describe the ECG

134. This is another example of  ventricular tachycardia , this time with a LBBB morphology (compare this with  ECG 046 ). Regular broad complex tachycardia at ~ 160 bpm. Features of VT in V1 : Initial R wave > 30 ms wide, RS interval > 70 ms (= Brugada sign). Features of VT in V6 : Dominant S wave in V6, absence of typical LBBB morphology. Abnormal axis with positive aVR , although does not quite meet criteria for  northwest axis . NB. Note that a positive Brugada sign only requires an RS interval of >70 ms when LBBB morphology is present, compared to >100 ms when RBBB morphology is present

135. Again, these features are very different to the expected pattern in  LBBB , which has: Dominant S wave in V1, but with an R/S interval < 70 ms and minimal initial R wave. Dominant R wave in V6 (often slurred)

136. Tips for Spotting VT when LBBB morphology present [NB. LBBB morphology = QRS > 120ms with dominant S wave in V1] Suspect VT in any patient with a regular broad complex tachycardia ( esp if > 160 ms wide ). Look at aVR Positive QRS complex? Leads I and aVF negative? If yes to both ->  northwest axis  is present -> probable VT. Look at V1 Initial R wave > 30 ms ? -> probable VT. Notching of the S wave (Josephson’s sign)? -> probable VT. RS interval > 70 ms ( Brugada’s sign)? -> probable VT. None of the above -> possible SVT with LBBB Look at V6 If still uncertain, scrutinise the ECG for: AV dissociation — P waves randomly deforming the QRS complexes and T waves. Fusion and capture beats.

137. ECG 048: 30-year old female presenting with sudden onset of palpitations. Normally well. Describe the ECG .

138. On first glance this would appear to be  SVT  with  LBBB  as there is: Regular broad-complex tachycardia. No atrial activity seen. Typical LBBB morphology in aVR , V1 and V6. No obvious diagnostic features for VT — compare this with  ECG 047 . However , there is  one feature  here that is unusual for LBBB, can you spot it? Answer There is an  inferior axis (+90 degrees) , which is atypical for LBBB. LBBB normally has a  leftward axis . This combination of… Broad complex tachycardia with typical LBBB morphology. Inferior axis (+90 degrees ). … is suggestive of a specific type of VT known as  right ventricular outflow-tract tachycardia  (RVOT).

139. RVOT is a relatively common form of right ventricular VT, occurring in two main groups : Patients with structurally normal hearts (= 70% of idiopathic VT). Patients with  arrhythmogenic right ventricular cardiomyopathy . It may be very difficult to differentiate RVOT from SVT with LBBB. [ NB. Left bundle branch block  morphology  simply indicates that the heart is depolarising from  right to left . Hence, similar QRS patterns are seen with  LBBB ,  RVOT  and  RV-pacing ] Tips for Spotting RVOT Suspect RVOT when you see LBBB morphology + inferior axis. Record a long rhythm strip looking for fusion and capture beats.

140. ECG 049: Elderly male presenting with dizziness. Describe the ECG

141. Main Abnormalities Broad complex tachycardia at ~ 120 bpm. Pacing spikes precede each QRS complex. LBBB morphology (dominant S wave in V1-2) indicates a pacing electrode in the  right   ventricle. Negative concordance  is seen in V1-6 (all precordial leads show negative complexes). This is an often-cited feature of VT, but also occurs with paced rhythms. It simply indicates that ventricular depolarisation is spreading from anterior to posterior (away from V1-6), e.g. due to a pacemaker electrode stimulating the anterior wall of the RV. These features are consistent with a  pacemaker malfunction  resulting in a rapid ventricular-paced rhythm. Differential Diagnosis The differential diagnosis of this rhythm includes: Pacemaker-mediated tachycardia Sensor-induced tachycardia Atrial tachycardia (e.g. sinus, AF) driving the pacemaker to its maximum rate — may be appropriate response to exercise, shock, sepsis, etc

142. Pacemaker Mediated Tachycardia (PMT) This is a re-entrant rhythm involving the pacemaker circuit. It behaves very much like the  atrioventricular re-entry tachycardia (AVRT)  seen with  WPW syndrome , except that in this case the “accessory pathway” is formed by the pacemaker circuit. PMT is triggered when ventricular impulses pass retrogradely through the AV node and depolarise the atria. This retrograde P wave is sensed by the pacemaker, which then immediately paces the ventricles. This is followed by another retrograde P wave that maintains the circus movement. This rhythm can be terminated by activating magnet mode (which switches off sensing), or by reprogramming the pacemaker box (e.g. increasing the refractory period to “block out” the retrograde P waves).

143. Sensor Induced Tachycardia (SIT) Modern pacemakers are programmed to allow increased heart rates in response to physiological stimuli such as exercise, tachypnoea , hypercapnia or acidaemia . Sensors may “misfire” in the presence of distracting stimuli such as vibrations, loud noises, fever, limb movement, hyperventilation or electrocautery (e.g. during surgery). This misfiring leads to pacing at an inappropriately fast rate. The ventricular rate cannot exceed the pacemaker’s upper rate limit. Similar to PMT, these may also terminate with application of a magnet, or with removal of the inciting stimulus Tips for Dealing with Rapid Paced Rhythms If the patient is attached to critical care monitoring, ensure that you  switch off respiratory impedence monitoring mode  (where the monitor senses respiratory rate via the ECG electrodes). This gives off an electrical signal that is  known to interfere with pacemakers . If this doesn’t work, try changing monitors to one that does not use respiratory impedance technology. Apply a magnet  to the pacemaker box. This activates  magnet mode , which resets the pacemaker to provide temporary asynchronous pacing (AOO, VOO or DOO). Arrange for an  urgent pacemaker check . A pacemaker technician may be able to adjust the settings to terminate the dysrhythmia and prevent its recurrence. If a pacemaker technician is not readily available, then a  trial of AV nodal blocking drugs  (e.g. beta blockers, verapamil) may be successful in terminating PMT.

144. ECG 050 : Elderly patient presenting with collapse. Clinically dehydrated. Describe the ECG.

145. This is a classic  sine wave  ECG of  critical  hyperkalaemia Bradycardia (~ 55 bpm). Bizarre-looking QRS complexes. Gross QRS prolongation (> 300 ms ). Massively peaked T waves. This patient had a K+ of 9.9 mmol /L! Clinical Pearls Any time you see an ECG that is… Blocked  (AV block, bundle branch block) Bradycardic  (sinus brady , slow AF, junctional bradycardia) Bizarre  in appearance … consider  hyperkalaemia  and check the K+ urgently!

146. ECG 051: 2-year old boy presenting with febrile seizure. Interpret the ECG.

147. ECG 51 answer This is a  normal paediatric ECG , displaying multiple age-appropriate features: Heart rate of 110 bpm (normal for age). Dominant R waves in V1-3. Partial RBBB (RSR’ pattern in V1). Juvenile T-wave pattern (T wave inversion in V1-3). Any of the following findings may be normal on the  paediatric ECG : Heart rate and rhythm Heart rate >100 beats/min. Marked sinus arrhythmia. Right-sided predominance Rightward QRS axis > +90° Dominant R wave in V1 RSR’ pattern in V1 T wave inversions in V1-3 (“juvenile T-wave pattern”)

148. P waves Slightly peaked P waves (< 3mm in height is normal if ≤ 6 months) Intervals Short PR interval (< 120ms) and QRS duration (<80ms) Slightly long QTc (≤ 490ms in infants ≤ 6 months) Pseudo-infarction patterns Q waves in the inferior and left precordial leads.

149. ECG 052: Middle-aged patient presenting with central chest pain. Now asymptomatic. Interpret the ECG.

150. This is classic ECG of  Wellens ’ syndrome ,  demonstrating characteristic biphasic T waves in V1-3 . This ECG pattern is highly predictive of a significant occlusive lesion of the LAD . The biphasic T waves are a marker of reperfusion and may occur after an aborted  anterior STEMI . Despite often being pain free and having normal cardiac enzymes at presentation, these patients are at risk of sudden LAD re-occlusion leading to massive anterior STEMI and are best managed with early angiography and PCI / CABG.

151. Clinical Pearls Biphasic T waves may be seen with both  Wellens ’ syndrome  and  hypokalaemia . The main differentiating factor (apart from the clinical picture) is the direction of the T waves: Wellens ’ biphasic T waves go UP then down . Hy pokalaemic T wav es go DOWN then up . Wellens ’ Syndrome Hypokalaemia

152.  ECG 053: Elderly patient presenting with nausea and palpitations. Interpret the ECG.

153. This rhythm is frequently misidentified as  atrial fibrillation . However, note in this case : Well-defined sawtooth waves in II, III, aVF with regular rate (~300bpm) and consistent morphology . Positive flutter waves (“pseudo-P waves”) in V1-2 . The rhythm is  not  irregularly irregular. There are repeating patterns of identical R-R intervals that crop up throughout the rhythm strip, corresponding to A V conduction ratios of either 2:1 or 4:1. This is  atrial flutter with a variable block . Recurring RR intervals in flutter with variable block

154. Clinical Pearls Misidentifying this rhythm as AF is not normally a big problem as both conditions are managed similarly — i.e. rate control, anticoagulation . However,  flutter will cardiovert with lower energy than AF  — e.g. 50 j compared with 100-200 j.

155. ECG 054: Elderly patient presenting with nausea and visual disturbance. Interpret the ECG.

156. This is a tricky ECG! There is evidence of  atrial fibrillation , as evidenced by the irregular baseline with fibrillatory waves most prominent in V1-2 . NB. Fibrillatory waves are characteristically seen in V1-2 (which overlie the atria), as opposed to  tremor artefact  which may be in seen in multiple leads without a predominance for V1-2 .   However, the ventricular rhythm is regular. How can this be? AF is irregular by definition… This is an example of  “ regularised AF”  due to  digoxin toxicity : The underlying rhythm is AF, which is being treated with digoxin. There is  complete heart block , prevent atrial impulses from reaching the ventricles. There is an  accelerated junctional rhythm  maintaining cardiac output. If this all seems like too much of a coincidence, then consider the pathophysiology of digoxin toxicity…

157. Mechanisms of Digoxin Toxicity Digoxin toxicity produces a wide variety of dysrhythmias, due to: Increased automaticity  of atrial, junctional and ventricular tissues — via actions at the Na/K and Na/Ca exchangers causing increased intracellular calcium and therefore increased spontaneous depolarisation of cardiac pacemaker cells. Decreased AV conduction  — via increased vagal tone at the AV node. Digoxin toxicity therefore usually produces some combination of: Increased atrial automaticity  — especially atrial tachycardia, but also  atrial ectopics ,  AF ,  flutter . Increased junctional automaticity  — especially  accelerated junctional rhythms . Increased ventricular automaticity  — frequent  VEBs and bigeminy ,  polymorphic VT . AV blocks  — including  1st ,  2nd  and  3rd degree  AV block. Characteristic ECG patterns include:

158. Atrial tachycardia with high-grade AV block   (= the classic dig-toxic rhythm). Regularised AF    =  AF with complete heart block + accelerated junctional escape rhythm, producing a paradoxically regular rhythm. Bidirectional VT   = polymorphic VT with QRS complexes that alternate between left- and right-axis-deviation, or between LBBB and RBBB morphology. NB . Digoxin toxicity should not be confused with  digoxin effect  (= “sagging” ST depression and T-wave inversion in patients on therapeutic doses of digoxin; not predictive of toxicity).  Clinical Pearls  Check for tremor artefact before you start diagnosing regularised AF! If the ECG pattern appears genuine and the clinical picture is compatible with digoxin toxicity (GI upset, xanthopsia , current digoxin treatment), then check an urgent digoxin level.

159. ECG 055: Middle-aged patient presenting with drowsiness. BP 85/50. Pupils dilated. Interpret the ECG.

160. ECG 55 answer Main Abnormalities This is a classic ECG of  tricyclic antidepressant toxicity , demonstrating multiple characteristic abnormalities. Signs of sodium-channel blockade Broad QRS complexes (120 ms , or 3 small squares). Positive R’ wave in lead aVR > 3 mm. Prolonged PR interval (240 ms ). Long QT interval (> 1/2 the RR interval). Brugada-like  pattern in V1 . Signs of anticholinergic toxidrome Sinus tachycard ia (~ 110 bpm), with P waves embe dded in each T wave. Positive R’ wave in aVR > 3mm P waves visible in V2 with long PR interval Pseudo-Brugada pattern in V1

161. This patient had taken a life-threatening overdose of dosulepin (a TCA). How to Spot Sodium-Channel Blockade QRS prolongation (> 100ms or 2.5 small squares), typically measured in lead II. A terminal or secondary R wave (R’ wave) in aVR > 3 mm. An R’/S ratio in aVR > 0.7. Prognostic Value of the ECG In patients with TCA overdose, the degree of QRS prolongation correlates with the degree of clinical toxicity: QRS width > 100 ms is predictive of seizures. QRS width > 160 ms is predictive of cardiotoxicity (e.g. broad-complex dysrhythmias, hypotension ). Clinical Pearls The combination of PR prolongation and sinus tachycardia with TCA overdose often makes the P waves difficult to see, and may lead the rhythm to be incorrectly identified as VT. This patient needs bicarbonate and hyperventilation, not electricity and amiodarone ! The clinical significance of a  TCA-induced Brugada ECG pattern r emains controversial — i.e. is it purely a manifestation of severe sodium-channel blockade, or does it represent “unmasking” of underlying  Brugada syndrome ? These issues are discussed  here .

162. ECG 056: Middle-aged patient presenting with drowsiness. Brief seizure in ED. BP unrecordable . Interpret the ECG.

163. This is a repeat ECG of the  previous patient  with  massive TCA overdose , taken a short while later . There is now evidence of advanced  sodium-channel blockade , with grossly prolonged QRS and QT intervals and further evolution of the R’ wave in aVR . The ECG is beginning to take on bizarre morphology and a sine wave appearance reminiscent of  severe hyperkalaemia . In some leads (II, III, aVF ), the QRS morphology resembles  ventricular tachycardia . These features are all due to sodium-channel blockade, and resolved following aggressive treatment with IV bicarbonate, intubation and hyperventilation.

164. post-treatment ECG Resolving TCA toxicity – QRS complexes narrowing and R’ wave disappearing with treatment.

165. Clinical Pearls  Advanced sodium-channel blockade can resemble either  VT  or  hyperkalaemia . Standard VT treatments such as DC cardioversion and amiodarone are likely to be ineffective and potentially harmful if the broad complex rhythm is due to sodium-channel blockade. Consider the clinical context and look for clues of TCA toxicity (e.g.  anticholinergic toxidrome ). In arrested / peri -arrest patients with a broad or bizarre-looking ECG, consider empirical treatment for both  hyperkalaemia  (with calcium) and  sodium-channel blockade  (with bicarbonate and hyperventilation).

166. ECG 057: Middle-aged patient presenting with chest pain and diaphoresis. Becomes unresponsive during recording of ECG. Interpret the ECG

167. Main Abnormalities This is a fascinating ECG with multiple abnormalities: The first half of the tracing shows a  ventricular paced rhythm  with positive  Sgarbossa criteria  indicating superimposed  inferior STEMI . There is  excessively discordant ST elevation  (> 25% of Q/S wave depth) in II, III and aVF with reciprocal change in I and aVL . A ventricular ectopic (beat #8) occurs at a vulnerable time, resulting in a run of  ventricular flutter  (very rapid VT at rates > 200-300 bpm). This rapidly degenerates to  ventricular fibrillation  (seen in the rhythm strip, which is recorded  after  the other 12 leads ). The artefact at the start of the rhythm strip may represent a precordial thump! Clinical Pearls While most rhythm strips are recorded simultaneously with the 12-lead ECG, some older machines may record the rhythm strip  after  the other 12 leads. Consider this as a possibility if your rhythm strip doesn’t seem to “line up” with the rest of the ECG.

168. ECG 058: Elderly patient presenting with chest pain. Interpret the ECG.

169. Main Abnormalities This ECG shows changes consistent with an old  anterolateral infarction  — the so-called  left ventricular aneurysm  pattern. ST elevation in V1-3 associated with deep Q waves (=  LV aneurysm morphology ). Pathological Q waves  also seen in I, aVL and V4. Poor R wave progression  (= R wave height < 3 mm in V3). Biphasic / inverted T waves in V1-5, I and aVL . Clinical Pearls The LV aneurysm pattern refers to the combination of residual ST elevation, deep Q waves and inverted or biphasic T waves seen in patients following an acute myocardial infarction. This ECG pattern is associated with transmural scarring and paradoxical movement of the LV on  wall on echocardiography. Around 60% of patients with anterior STEMI develop some degree of chronic ST elevation on their ECG, which can cause diagnostic confusion. If these patients present with chest pain, the safest approach is to take serial ECGs looking for signs of evolving STEMI such as evolving ST elevation or  pseudo- normalisation of T waves .

170. ECG 059: 57-year old man with ROSC following VF arrest. Interpret the ECG. http://lifeinthefastlane.com/ecg-library/100-ecgs/quiz-ecg-059/

171. ECG 5 9 answer Main Abnormalities Sinus rhythm with frequent ventricular ectopics in a pattern of  ventricular bigeminy . Grossly prolonged QT interval (> 600 ms ). “ R on T” phenomenon is present, with each VEB falling on the end of the T wave — this ECG pattern is very high risk for deterioration to  torsades de pointes  and  ventricular fibrillation . Relatively short PR interval and possible  delta waves  (leads I, II, V6) are suggestive — but not diagnostic — of  WPW syndrome . Voltage criteria for  left ventricular hypertrophy  are present in multiple leads. This patient had suffered a cardiac arrest in the context of severe  hypertrophic cardiomyopathy  and  long QT syndrome . ( NB. ~1/3 of patients with HOCM will have some evidence of WPW on their ECG ). Can you guess what happened next? The patient had a further TdP cardiac arrest! This was treated with IV magnesium and potassium, with restoration of sinus rhythm .

172. ECG 060: 16-year old male presenting with syncope. Describe and interpret his ECG.

173. ECG 060 answer Main Abnormalities Markedly peaked T waves in V2-6. Extremely short QT interval (~240 ms ). In a patient presenting with syncope, this ECG pattern is very suspicious for the  short QT syndrome . Short QT Syndrome This is a recently-described arrhythmogenic condition associated with paroxysmal  atrial  and  ventricular fibrillation . The hallmark is a significantly shortened QT interval (at least < 360 ms , often < 330 ms ) with associated T-wave peaking. SQTS is a genetically-inherited  cardiac channelopathy  on the same spectrum as other familial arrhythmogenic diseases such as  Long QT Syndrome  (LQTS),  Brugada Syndrome  and  Catecholaminergic Polymorphic  Ventricular Tachycardia  (CPVT ).

174. When to Suspect SQTS Any patient with a QT interval < 330 ms. QT interval < 360 ms and convincing symptoms (syncope, cardiac arrest) or family history. Differential Diagnosis Peaked T waves and short QT interval may be seen with  severe hyperkalaemia . A shortened QT interval may also be seen with  severe hypercalcaemia .

175. ECG 061: Middle-aged patient presenting with an episode of chest pain. Currently asymptomatic. Describe and interpret his ECG

176. ECG 060 answer This pattern of deeply inverted T waves in the anterolateral leads V2-6, I and aVL is characteristic of  Wellens syndrome . This ECG pattern is highly predictive of a significant occlusive lesion of the LAD. The inverted T waves are a marker of reperfusion and may occur after an aborted  anterior STEMI . Despite often being pain free and having normal cardiac enzymes at presentation, these patients are at risk of sudden LAD re-occlusion leading to massive anterior STEMI and are best managed with early angiography and PCI / CABG. Differential Diagnosis A similar pattern of deep anterolateral T-wave inversions may also be seen with: Apical  hypertrophic cardiomyopathy  – suspect if associated  LVH Raised intracranial pressure  – patient will be comatose (see  Quiz ECG #12 )

177. ECG 062: Middle aged patient presenting with chest pain and diaphoresis. Describe and interpret his ECG

178. Main Abnormalities ST depression in V2-6, which slopes upwards and joins the ascending limb of the T wave. Prominent, “rocket-shaped” T waves in the precordial leads V2-5. Subtle ST elevation in aVR . Diagnosis This combination of ST depression with rocket-shaped T waves in the precordial leads V1-6 is referred to as the De Winter ECG pattern or  “De Winter’s T waves”  (also see  ECG #19 ) It is becoming increasingly recognised as an anterior STEMI equivalent (~2% of LAD occlusions). Some authors  are now recommending that this ECG pattern be treated identically to anterior STEMI, with urgent PCI or thrombolysis.

179. ECG 063: Elderly patient presenting with reduced level of consciousness, hypothermia and hypotension refractory to inotropes. Describe and interpret his ECG

180. The most striking abnormality on this ECG is  extremely low QRS voltage , in this case due to  severe myxoedema . Definition The QRS is said to be low voltage when: The amplitudes of all the QRS complexes in the limb leads are < 5 mm; or The amplitudes of all the QRS complexes in the precordial leads are  < 10 mm Mechanisms Low voltage is produced by… The “damping” effect of increased layers of fluid, fat or air between the heart and the recording electrode. Loss of viable myocardium. Diffuse infiltration or myxoedematous involvement of the heart. Causes: Specific causes of low voltage include: a) Fluid Pericardial effusion Pleural effusion b) Fat Obesity

181. c) Air Emphysema Pneumothorax d) Infiltrative / Connective Tissue Disorders Myxoedema Infiltrative myocardial diseases — i.e.  restrictive cardiomyopathy  due to amyloidosis, sarcoidosis, haemochromatosis Constrictive pericarditis Scleroderma e) Loss of viable myocardium Previous massive MI End-stage  dilated cardiomyopathy The most important cause is massive pericardial effusion, which produces a triad of: Low voltage Tachycardia Electrical alternans

182. Quiz ECG 064 Chest pain and diaphoresis. BP 80/50 . Describe and interpret his ECG

183. Key Abnormalities There is ST elevation in the inferior leads II, III and aVF . The concave morphology might lead you to suspect  pericarditis  — however, there is reciprocal change in the high lateral leads I and aVL , confirming the diagnosis of  inferior STEMI . There are additional features suggestive of  right ventricular infarction : ST elevation in III > II Isoelectric ST segment in V1 with ST depression in V2 Other Abnormalities There is a break in the rhythm towards the end of the rhythm strip, with what appears to be a non-conducted P wave, suggesting the development of  2nd degree AV block  — e.g. a slowly-evolving  Wenckbach cycle . The 13th QRS complex appears to be a supraventricular ectopic beat ( PAC  or  PJC ).

184. Quiz ECG 065 Chest pain and diaphoresis. BP 80/50. Describe and interpret his ECG

185. This is a repeat ECG of the  previous patient , demonstrating: Inferior STEMI  — STE in II, III, aVF with reciprocal change in I and aVL . Evidence suggesting  RV infarction  — STE in III > II. Evidence confirming  RV infarction  — STE and  hyperacute T wave  in V4R. Evolving second degree AV block with alternating  2:1 block  and  3:2 Wenckebach cycles . This ECG pattern is diagnostic of a right coronary artery occlusion. Rhythm Strip Explanation Arrows indicate the position of P waves. Black arrrows indicate conducted P waves. Red arrows indicate  non-conducted  P waves — some of these are concealed within the preceding T wave, causing a small bump at the back of the T wave. Complexes cluster together in groups with either  2:1 conduction  or as  3:2 Wenckeback cycles , with prolongation of the PR interval prior to the non-conducted P wave. The number above each P wave denotes its position in the sequence.

186. Bradycardia and AV Block in Inferior STEMI Up to 20% of patients with inferior STEMI will develop either second- or third degree heart block. There are two presumed mechanisms for this : Ischaemia of the AV node  due to impaired blood flow via the  AV nodal artery . This artery arises from the RCA 80% of the time, hence its involvement in inferior STEMI due to RCA occlusion. Bezold-Jarisch reflex  = increased vagal tone secondary to ischaemia . The conduction block may develop either as a step-wise progression from  1st degree heart block  via  Wenckebach  to  complete heart block  (in 50% of cases) or as abrupt onset of second or third-degree heart block (in the remaining 50%). Patients may also manifest signs of sinus node dysfunction, such as sinus bradycardia, sinus pauses,  sinoatrial exit block  and sinus arrest. Similarly to AV node dysfunction, this may result from increased vagal tone or ischaemia of the SA node (the SA nodal artery is supplied by the RCA in 60% of people). Bradyarrhythmias and AV block in the context of inferior STEMI are usually transient (lasting hours to days), respond well to atropine and do not require permanent pacing.

187. Quiz ECG 066 Elderly patient presenting with chest pain and diaphoresis. Describe and interpret his ECG

188. This ECG demonstrates an  infero -posterior STEMI , as manifest by: Subtle  inferior STE  and hyperacute T waves (T waves > QRS complexes) ST depression and terminal T-wave positivity in V2-3 =  posterior wall involvement See  Quiz ECG 14  for another example of posterior infarction.  Tips for spotting posterior infarction Look specifically at leads V2-3 for the combination of: Horizontal ST depression. Tall, broad R wave (>30ms wide, R/S ratio > 1) — this is a Q-wave equivalent. Upright T wave — particularly the terminal portion of the T wave. One common trick is to turn the ECG over, hold it up to the light and look through it from behind. This inverts lead V2, which then takes on the appearance of a classic STEMI. Typical appearance of posterior infarction in V2-3

189. In this ECG example, V3 is the most characteristically abnormal lead . Look for evidence of posterior involvement in any patient with an  inferior  or  lateral STEMI . Sometimes it can be difficult to determine whether ST depression in V2-3 is due to posterior STEMI or simply subendocardial ischaemia affecting the anteroseptal wall. The diagnosis can be confirmed by recording  posterior leads V7-9 .

190. Quiz ECG 067 Elderly patient with chest pain and diaphoresis. Describe and interpret his ECG

191. This is the same patient as  ECG 066 . Posterior leads V7-9  show subtle ST elevation with early Q-wave formation, confirming the presence of  posterior infarction .

192. Quiz ECG 068 Severe chest pain and hypotension (70/40) in an elderly man. Describe and interpret his ECG

193. This ECG shows: ST elevation in aVR . ST depression in multiple leads (V5-6, I, II, aVL , aVF ). Evidence of  anteroseptal STEMI  – ST elevation with Q wave formation in V1-3. In the context of ischaemic chest pain and cardiogenic shock, the combination of… Widespread ST depression ST elevation in aVR > 1 mm ST elevation in V1-3 … is concerning for  proximal LAD occlusion  (compare this to the  LMCA pattern  seen in  Quiz ECG 008 ). While this pattern of diffuse ST depression with STE in aVR if often referenced as a marker of  LMCA / proximal LAD occlusion ,  may be seen

194. While this pattern of diffuse ST depression with STE in aVR if often referenced as a marker of  LMCA / proximal LAD occlusion ,  may be seen whenever there is diffuse severe subendocardial ischaemia, e.g. Severe triple vessel disease Severe anaemia or hypoxaemia Following resuscitation from cardiac arrest Outcome This patient actually had  severe multi-vessel disease . Angiography demonstrated a chronic total occlusion of his circumflex artery, with critical stenoses of his proximal LAD, RCA and ramus intermedius. Surprisingly, in this case the culprit vessel was thought to be the RCA, which had been collateralising his chronically occluded circumflex. He went on to receive a CABG x 4.

195. Quiz ECG 069 18-year old female with severe traumatic brain injury, ICP 40mmHg. Fluctuating BPs. Describe and interpret her ECG

196. The ECG shows diffuse ST elevation. The morphology is atypical, there is no clear anatomical predominance for a vascular territory and no obvious reciprocal changes (except the inverted leads V1 and aVR ). This is an example of a pseudo-infarction pattern due to  raised intracranial pressure . Compare this with  Quiz ECG 012  (raised ICP causing giant T wave inversions). ECG changes with elevated ICP Raised ICP is associated with certain characteristic ECG changes: Widespread giant  T-wave inversions  (“cerebral T waves”). QT prolongation . Bradycardia  (the  Cushing reflex  – indicates imminent brainstem herniation).

197. Other possible ECG changes that may be seen: ST segment elevation / depression —  this may mimic myocardial ischaemia or pericarditis. Increased  U wave  amplitude. Other rhythm disturbances: sinus tachycardia, junctional rhythms, premature ventricular contractions, atrial fibrillation . In some cases, these ECG abnormalities may be associated with echocardiographic evidence of regional ventricular wall motion abnormality — so-called  neurogenic stunned myocardium  or  neurogenic stress cardiomyopathy . The presumed mechanism is massive release of catecholamines , similar to  Takutsubo syndrome . This patient developed labile blood pressures and transient wall motion abnormalities plus these ECG changes during a sustained spike in her ICP. The ECG changes and wall motion abnormalities improved once her ICPs came under control .

198. Quiz ECG 070 Elderly patient presenting with sudden onset of chest pain and shortness of breath. Hypoxic (SaO2 82% RA) and hypotensive (80/50). Describe and interpret his ECG

199. There are multiple features suggestive of  right ventricular hypertrophy  or  strain : Right axis deviation Dominant R wave in V1 Right bundle branch block Right ventricular strain pattern  — T wave inversions in V1-4, lead III S I  Q III  T III   pattern Clockwise rotation of the heart , with a persistent S wave in V6 Given the clinical history, the most likely scenario is  acute right heart strain  due to  massive pulmonary embolism . A similar ECG pattern may also be seen with  chronic cor pulmonale , pulmonary hypertension or  RV hypertrophy (e.g. due to congenital heart disease ) . ECG changes in pulmonary embolism include: Sinus tachycardia  –  the most common abnormality; seen in 44% of patients. Complete or incomplete RBBB  –  associated with increased mortality; seen in 18% of patients.

200. Right ventricular strain pattern  –   T wave inversions in the right precordial leads (V1-4) ± the inferior leads (II, III, aVF ). This pattern is seen in up to 34% of patients and is associated with high pulmonary artery pressures. Right axis deviation  – seen in 16% of patients. Extreme right axis deviation may occur, with axis between zero and -90 degrees, giving the appearance of left axis deviation (“pseudo left axis”). Dominant R wave in V1   – a manifestation of acute right ventricular dilatation. Right atrial enlargement (P pulmonale )  –  peaked P wave in lead II > 2.5 mm in height. Seen in 9% of patients . S I  Q III  T III   pattern  – deep S wave in lead I, Q wave in III, inverted T wave in III. This “classic” finding is neither sensitive nor specific for pulmonary embolism; found in only 20% of patients with PE . Clockwise rotation  –  shift of the R/S transition point towards V6 with a persistent S wave in V6 (“pulmonary disease pattern”), implying rotation of the heart due to right ventricular dilatation . Atrial tachyarrhythmias –   AF ,  flutter ,  atrial tachycardia . Seen in 8% of patients. Non-specific ST segment and T wave changes , including ST elevation and depression. Reported in up to 50% of patients with PE. Simultaneous T wave inversions in the inferior (II, III, aVF ) and right precordial leads (V1-4) is the most specific finding in favour of PE. 

201. Quiz ECG 071 Palpitations. Describe and interpret this ECG

202. QRS alternans – due to  AVNRT  (i.e. electrical phenomenon), not  pericardial effusion  as normal voltages.

203. Quiz ECG 072 Palpitations, chest heaviness

204. Rate-related ST change with  SVT  = not necessarily ischaemic. Mimics appearance of  LMCA occlusion .

205. Quiz ECG 073 Pleuritic chest pain after weight lifting. Describe and interpret this ECG

206. Benign Early Repolarisation https://lifeinthefastlane.com/ecg-library/benign-early-repolarisation/